Cardiovascular disease is one of the leading causes of death worldwide. For example, some recent studies have suggested that plaque rupture may trigger 60 to 70% of fatal myocardial infarctions. In a further 25 to 30% of fatal infarctions, plaque erosion or ulceration is the trigger. Vulnerable plaques are often undetectable using conventional techniques such as angiography. Indeed, the majority of these vulnerable plaques that lead to infarction occur in coronary arteries that appeared normal or only mildly stenotic on angiograms performed prior to the infarction.
Studies into the composition of vulnerable plaque suggest that the presence of inflammatory cells (and particularly a large lipid core with associated inflammatory cells) is the most powerful predictor of ulceration and/or imminent plaque rupture. For example, in plaque erosion, the endothelium beneath the thrombus is replaced by or interspersed with inflammatory cells. Recent literature has suggested that the presence of inflammatory cells within vulnerable plaque and thus the vulnerable plaque itself, might be identifiable by detecting heat associated with the metabolic activity of these inflammatory cells. Specifically, it is generally known that activated inflammatory cells have a heat signature that is slightly above that of connective tissue cells. Accordingly, it is believed that one way to detect whether specific plaque is vulnerable to rupture and/or ulceration is to measure the temperature of the plaque walls of arteries in the region of the plaque.
Once vulnerable plaque is identified, the expectation is that in many cases it may be treated. Since currently there are not satisfactory devices for identifying vulnerable plaque, current treatments tend to be general in nature. For example, low cholesterol diets are often recommended to lower serum cholesterol (i.e. cholesterol in the blood). Other approaches utilize systemic anti-inflammatory drugs such as aspirin and non-steroidal drugs to reduce inflammation and thrombosis. However, it is believed that if vulnerable plaque can be reliably detected, localized treatments may be developed to specifically address the problems.
In view of the foregoing, improved catheters that facilitate the identification, location and mapping of inflamed plaque and/or other hot spots within arteries and/or other vessels would be desirable. Further, integrated catheter devices which are capable of both locating vulnerable plaque and delivering appropriate treatment agents would be desirable.